Signal transmission at synapses is mediated by the neurotransmitter acetylcholine. Such signaling may be discontinued by AChE, which catalyzes the hydrolysis of acetylcholine. AChE-inhibiting chemicals may prevent the breakdown of acetylcholine, thereby disrupting normal nervous system activity through an excess of acetylcholine at synapses. For example, certain classes of pesticides, such as organophosphates and carbamates, may result in toxicity through AChE inhibition. Organophosphate chemical warfare agents such as sarin and tabun also function through AChE inhibition. Accordingly, if an individual may be exposed to such inhibitors, there remains a need to prophylactically or therapeutically mitigate or reverse such cholinergic toxicity. Individuals or animals who have been exposed to a cholinesterase inhibitor may currently be treated with an AChE reactivator (antidote) such as pralidoxime in combination with atropine, a competitive agonist for acetylcholine at muscarinic receptors, and an anti-seizure medication such as benzodiazepine. In addition, AChE reactivators may be employed medicinally to treat various ailments such as Alzheimer's disease.